Origin and role of distal visceral endoderm, a group of cells that determines anterior–posterior polarity of the mouse embryo

2011 ◽  
Vol 13 (7) ◽  
pp. 743-752 ◽  
Author(s):  
Katsuyoshi Takaoka ◽  
Masamichi Yamamoto ◽  
Hiroshi Hamada
Keyword(s):  
Mouse Embryo ◽  
Visceral Endoderm ◽  
Anterior Posterior

HNF3beta and Lim1 interact in the visceral endoderm to regulate primitive streak formation and anterior-posterior polarity in the mouse embryo

Development ◽  
1999 ◽  
Vol 126 (20) ◽  
pp. 4499-4511 ◽  
Author(s):  
A. Perea-Gomez ◽  
W. Shawlot ◽  
H. Sasaki ◽  
R.R. Behringer ◽  
S. Ang
Keyword(s):  
Mouse Embryo ◽  
Primitive Streak ◽  
Axis Formation ◽  
Visceral Endoderm ◽  
Primary Defect ◽  
Homozygous Mutant ◽  
Early Mouse ◽  
Mesoderm Patterning ◽  
Anterior Posterior ◽  
Anterior Visceral Endoderm

Recent embryological and genetic experiments have suggested that the anterior visceral endoderm and the anterior primitive streak of the early mouse gastrula function as head- and trunk-organising centers, respectively. Here, we report that HNF3beta and Lim1 are coexpressed in both organising centers suggesting synergistic roles of these genes in regulating organiser functions and hence axis development in the mouse embryo. To investigate this possibility, we generated compound HNF3beta and Lim1 mutant embryos. An enlarged primitive streak and a lack of axis formation were observed in HNF3beta (−)(/)(−);Lim1(−)(/)(−), but not in single homozygous mutant embryos. Chimera experiments indicate that the primary defect in these double homozygous mutants is due to loss of activity of HNF3beta and Lim1 in the visceral endoderm. Altogether, these data provide evidence that these genes function synergistically to regulate organiser activity of the anterior visceral endoderm. Moreover, HNF3beta (−)(/)(−);Lim1(−)(/)(−) mutant embryos also exhibit defects in mesoderm patterning that are likely due to lack of specification of anterior primitive streak cells.

scholarly journals The role of Pten in anterior–posterior (AP) axis formation in the mouse embryo

2008 ◽  
Vol 319 (2) ◽  
pp. 584
Author(s):  
Joshua E. Bloomekatz ◽  
Andrew Rakeman ◽  
Heather Alcorn ◽  
Kathryn V. Anderson
Keyword(s):  
Mouse Embryo ◽  
Axis Formation ◽  
Anterior Posterior

scholarly journals Heading forwards: anterior visceral endoderm migration in patterning the mouse embryo

2014 ◽  
Vol 369 (1657) ◽  
pp. 20130546 ◽  
Author(s):  
Matthew J. Stower ◽  
Shankar Srinivas
Keyword(s):  
Epithelial Cells ◽  
Early Development ◽  
Mouse Embryo ◽  
Visceral Endoderm ◽  
Coordinated Action ◽  
Specialized Population ◽  
The Brain ◽  
Anterior Posterior ◽  
Anterior Visceral Endoderm

The elaboration of anterior–posterior (A–P) pattern is one of the earliest events during development and requires the precisely coordinated action of several players at the level of molecules, cells and tissues. In mammals, it is controlled by a specialized population of migratory extraembryonic epithelial cells, the anterior visceral endoderm (AVE). The AVE is a signalling centre that is responsible for several important patterning events during early development, including specifying the orientation of the A–P axis and the position of the heart with respect to the brain. AVE cells undergo a characteristic stereotypical migration which is crucial to their functions.

Hematopoietic induction and respecification of A-P identity by visceral endoderm signaling in the mouse embryo

Development ◽  
1998 ◽  
Vol 125 (24) ◽  
pp. 5009-5018 ◽  
Author(s):  
M. Belaoussoff ◽  
S.M. Farrington ◽  
M.H. Baron
Keyword(s):  
Mouse Embryo ◽  
Decisive Role ◽  
Primitive Streak ◽  
Explant Culture ◽  
Cell Contact ◽  
Primitive Endoderm ◽  
Cell Fates ◽  
Posterior Aspect ◽  
Anterior Posterior

The anteroposterior axis of the developing embryo becomes morphologically apparent at the onset of gastrulation with the formation of the primitive streak. This structure, where the first mesodermal cells arise, marks the posterior aspect of the embryo. To examine the potential role of non-mesodermal signals in specifying posterior (hematopoietic and endothelial) cell fates in the mouse embryo, we have devised a transgenic explant culture system. We show that interactions between primitive endoderm and adjacent embryonic ectoderm or nascent mesoderm are required early in gastrulation for initiation of hematopoiesis and vasculogenesis. Surprisingly, primitive endoderm signals can respecify anterior (prospective neural) ectoderm to a posterior mesodermal fate, resulting in formation of blood and activation of endothelial markers. Reprogramming of anterior ectoderm does not require cell contact and is effected by stage-dependent, short-range, diffusible signal(s). Therefore, primitive endoderm signaling is a critical early determinant of hematopoietic and vascular development and plays a decisive role in anterior-posterior patterning during mouse embryogenesis.

scholarly journals Antagonism between Smad1 and Smad2 signaling determines the site of distal visceral endoderm formation in the mouse embryo

2009 ◽  
Vol 184 (2) ◽  
pp. 323-334 ◽  
Author(s):  
Masamichi Yamamoto ◽  
Hideyuki Beppu ◽  
Katsuyoshi Takaoka ◽  
Chikara Meno ◽  
En Li ◽  
...  
Keyword(s):  
Mouse Embryo ◽  
Early Stage ◽  
Distal Region ◽  
Bmp Signaling ◽  
Visceral Endoderm ◽  
Inverse Relation ◽  
Primitive Endoderm ◽  
Dual Roles ◽  
Morphogenetic Protein ◽  
Anterior Posterior

The anterior–posterior axis of the mouse embryo is established by formation of distal visceral endoderm (DVE) and its subsequent migration. The precise mechanism of DVE formation has remained unknown, however. Here we show that bone morphogenetic protein (BMP) signaling plays dual roles in DVE formation. BMP signaling is required at an early stage for differentiation of the primitive endoderm into the embryonic visceral endoderm (VE), whereas it inhibits DVE formation, restricting it to the distal region, at a later stage. A Smad2-activating factor such as Activin also contributes to DVE formation by generating a region of VE positive for the Smad2 signal and negative for Smad1 signal. DVE is thus formed at the distal end of the embryo, the only region of VE negative for the Smad1 signal and positive for Smad2 signal. An inverse relation between the level of phosphorylated Smad1 and that of phosphorylated Smad2 in VE suggests an involvement of antagonism between Smad1- and Smad2-mediated signaling.

scholarly journals Interactions between the WEE-1.3 kinase and the PAM-1 aminopeptidase in oocyte maturation and the early C. elegans embryo

2021 ◽  
Author(s):  
Dorothy Benton ◽  
Eva C Jaeger ◽  
Arielle Kilner ◽  
Ashley Kimble ◽  
Josh Lowry ◽  
...  
Keyword(s):  
Missense Mutation ◽  
Oocyte Maturation ◽  
Protective Role ◽  
C Elegans ◽  
Direct Target ◽  
The One ◽  
Actomyosin Cytoskeleton ◽  
Embryonic Viability ◽  
Anterior Posterior

Abstract Puromycin-sensitive aminopeptidases are found across phyla and are known to regulate the cell-cycle and play a protective role in neurodegenerative disease. PAM-1 is a puromycin-sensitive aminopeptidase important for meiotic exit and polarity establishment in the one-cell Caenorhabditis elegans embryo. Despite conservation of this aminopeptidase, little is known about its targets during development. In order to identify novel interactors, we conducted a suppressor screen and isolated four suppressing mutations in three genes that partially rescued the maternal-effect lethality of pam-1 mutants. Suppressed strains show improved embryonic viability and polarization of the anterior-posterior axis. We identified a missense mutation in wee-1.3 in one of these suppressed strains. WEE-1.3 is an inhibitory kinase that regulates maturation promoting factor. While the missense mutation suppressed polarity phenotypes in pam-1, it does so without restoring centrosome-cortical contact or altering the cortical actomyosin cytoskeleton. To see if PAM-1 and WEE-1.3 interact in other processes, we examined oocyte maturation. While depletion of wee-1.3 causes sterility due to precocious oocyte maturation, this effect was lessened in pam-1 worms, suggesting that PAM-1 and WEE-1.3 interact in this process. Levels of WEE-1.3 were comparable between wild-type and pam-1 strains, suggesting that WEE-1.3 is not a direct target of the aminopeptidase. Thus, we have established an interaction between PAM-1 and WEE-1.3 in multiple developmental processes and have identified suppressors that are likely to further our understanding of the role of puromycin-sensitive aminopeptidases during development.

scholarly journals The Role of White Matter Disconnection in the Symptoms Relating to the Anarchic Hand Syndrome: A Single Case Study

2021 ◽  
Vol 11 (5) ◽  
pp. 632
Author(s):  
Valentina Pacella ◽  
Giuseppe Kenneth Ricciardi ◽  
Silvia Bonadiman ◽  
Elisabetta Verzini ◽  
Federica Faraoni ◽  
...  
Keyword(s):  
White Matter ◽  
Single Case ◽  
Brain Lesion ◽  
Structural Connectivity ◽  
Disconnection Syndrome ◽  
Neuroimaging Data ◽  
Neuropsychological Investigation ◽  
Anterior Posterior

The anarchic hand syndrome refers to an inability to control the movements of one’s own hand, which acts as if it has a will of its own. The symptoms may differ depending on whether the brain lesion is anterior, posterior, callosal or subcortical, but the relative classifications are not conclusive. This study investigates the role of white matter disconnections in a patient whose symptoms are inconsistent with the mapping of the lesion site. A repeated neuropsychological investigation was associated with a review of the literature on the topic to identify the frequency of various different symptoms relating to this syndrome. Furthermore, an analysis of the neuroimaging regarding structural connectivity allowed us to investigate the grey matter lesions and white matter disconnections. The results indicated that some of the patient’s symptoms were associated with structures that, although not directly damaged, were dysfunctional due to a disconnection in their networks. This suggests that the anarchic hand may be considered as a disconnection syndrome involving the integration of multiple antero-posterior, insular and interhemispheric networks. In order to comprehend this rare syndrome better, the clinical and neuroimaging data need to be integrated with the clinical reports available in the literature on this topic.

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